Gene interactions and pathways from curated databases and text-mining

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BIRC7 — CASP7

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Kasof et al., J Biol Chem 2001 : In addition, the unprocessed and cleaved forms of caspase-9 co-immunoprecipitated with Livin in vivo, and recombinant Livin could inhibit the activation of caspase-9 induced by Apaf-1, cytochrome c, and dATP
Vucic et al., J Biol Chem 2002 : Here we show that melanoma IAP (ML-IAP) , a potent anti-cell death protein and caspase inhibitor , physically interacts with SMAC through its BIR ( baculovirus IAP repeat ) domain
Yan et al., J Dermatol Sci 2006 (Melanoma) : Proteolytic cleavage of Livin ( ML-IAP ) in apoptotic melanoma cells potentially mediated by a non-canonical caspase
Das et al., Cancer 2007 (Glioblastoma) : Other events in apoptosis included overexpression of Bax, down-regulation of Bcl-2 and some BIRC proteins, mitochondrial release of cytochrome c and Smac into the cytosol, and activation of calpain, caspase-9 , and caspase-3
Das et al., Brain Res 2008 (Brain Neoplasms...) : Besides, apoptosis was associated with alterations in expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins resulting in an increase in Bax : Bcl-2 ratio, mitochondrial release of cytochrome c and Smac, downregulation of selective baculoviral inhibitor-of-apoptosis repeat containing ( BIRC ) molecules, an increase in intracellular free [Ca2+ ], and activation of calpain and caspase-3
Karmakar et al., Neuroscience 2009 (Body Weight...) : Combination of 4-HPR and GST increased Bax : Bcl-2 ratio, mitochondrial release of Smac, downregulation of baculovirus inhibitor-of-apoptosis repeat containing ( BIRC ) proteins including BIRC-2 and BIRC-3, and activation of caspase-3 and apoptosis inducing factor ( AIF )
Ding et al., Tumour Biol 2013 (Colonic Neoplasms) : The stable overexpression of Livin inhibited the activation of caspase-3 and led to resistance to cisplatin, while the knockdown of Livin by siRNA rendered colon cancer cells more sensitive to cisplatin